Interleukin-18 and its three gene polymorphisms relating to allergic rhinitis
Jazyk angličtina Země Velká Británie, Anglie Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
17252172
DOI
10.1007/s10038-006-0093-2
PII: 10.1007/s10038-006-0093-2
Knihovny.cz E-zdroje
- MeSH
- celoroční alergická rýma genetika MeSH
- dospělí MeSH
- genetická predispozice k nemoci MeSH
- genotyp MeSH
- imunoglobulin E krev MeSH
- interleukin-18 genetika MeSH
- jednonukleotidový polymorfismus genetika MeSH
- lidé MeSH
- polymerázová řetězová reakce MeSH
- polymorfismus délky restrikčních fragmentů MeSH
- sezónní alergická rýma genetika MeSH
- studie případů a kontrol MeSH
- Check Tag
- dospělí MeSH
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- imunoglobulin E MeSH
- interleukin-18 MeSH
The study aimed to examine an association of three different single nucleotide polymorphisms (SNPs) of the IL-18 gene (-607 C/A, -137 G/C and -133 C/G) on chromosome 11q22 with allergic rhinitis (AR). Genotyping for the SNPs was performed using 539 patients with AR and 312 healthy control volunteers. Positivity to the skin prick test for the fungus Alternaria sp. in patients with AR, and IgE levels according to particular genotypes of selected SNPs, were also determined. There were no significant differences in the distribution of single IL-18 alleles or genotypes between controls and AR patients. However, frequencies of combined IL-18 genotypes arising from combinations of the three common polymorphisms (-607, -137 and -133) were significantly different between both groups (P = 0.009, P (corr) < 0.05, OR = 5.35, 95% CI: 1.9-15.2). There was a marginally significant association of the IL-18-607 variant with IgE levels (P = 0.05) in patients, but not in the case of the other SNPs. Patients allergic to Alternaria, but not those allergic to other antigens, showed a significant association with the IL-18-607 polymorphism (P = 0.0037, P (corr) < 0.05). Results suggest that IL-18 gene variants may be one of the factors participating in the pathogenesis of AR or its intermediary phenotypes.
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